MULTIGLAKDULAR SYNDROMES 901 



histologic and pathologic findings in such hypoplastic conditions referable 

 to underactive or inhibited suprarenal glands. Many observers have de^- 

 scribed the smallness of the sell a turcica. Timme's observations agree 

 with theso. All of the cases show the smallness of the sella turcica in the 

 early stages and, in addition, many of them have the bridging over by the 

 clinoid processes, evident on x-ray examination. With these deficiencies 

 of glandular structure and their diminished potential physiologic activity 

 from the outset, the organism would of necessity come to early grief if 

 some corrective were not forthcoming. Many patients do succumb early. 

 Undue exertion, sudden excitement, narcosis, are all critical moments for 

 such organizations, many of which cannot survive them. After puberty 

 should have been reached (the second stage) the deficiency of the gonadal 

 inhibition to growth (Tandler and Grosz) is claimed to be responsible for 

 the extreme height rapidly reached in these cases. One of the patients 

 (Private B., Fig. 5), however, rather opposes this theory, in that the 

 gonadal system early became hyperplastic and still the growth in bodyj took 

 place. This excessive genital development may be due in his case to an 

 early involution of the pineal gland, for in the .T-ray calcification of the 

 pineal is seen. (Some authors hold that the overactive thymus with 

 disturbed calcium metabolism is the cause of such "thymic gigantism.") 

 The deficient adrenal-chromaffin system is to be credited with the great 

 fatiguability, the low blood sugar content, the low blood pressure and the 

 white line. Now comes the third stage, the all-important one. It is in 

 this period that the outcome of the syndrome is determined. In our 

 judgment it is the pituitary gland which is here the critical factor. As we 

 have seen, it is invariably enclosed in a small sella turcica. and possibly 

 even hemmed in by the clinoids. Among its functions we have as all 

 important a blood pressor principle and a sugar mobilization factor. Both 

 of these are deficient in our patient. If the pituitary possibly could be- 

 come hyperplastic and hyperactive with an intensification of these im- 

 portant properties, compensation might be accomplished. Such tendency 

 to hyperplasia in a small cavity would of necessity, through pressure, pro- 

 duce headaches an invariable symptom in the third stage of -the com- 

 pensated cases. And such headache would continue until the enlarged 

 gland through erosion of its bony capsule or through pushing apart the 

 clinoids made sufficient room for itself. As will be seen, these headaches 

 continue for two to ten years in some of the cases. Synchronously with 

 these headaches, other incidental features of an enlarged pituitary gland 

 become manifest: (a) acromegaly, developing until the headaches cease 

 and the process then likewise ceasing; (b) a higher blood sugar content; 

 (c) a higher blood pressure; (d) a diminished sugar tolerance. To make 

 this view of the nature of the process of compensation more tenable many 

 of the sellae turcicse of the patients in the second and third stages show 



